Distinct features of the host-parasite interactions between nonadherent and adherent Trichomonas vaginalis isolates

Abstract

Cytoadherence of Trichomonas vaginalis to human vaginal epithelial cells (hVECs) was previously shown to involve surface lipoglycans and several reputed adhesins on the parasite. Herein, we report some new observations on the host-parasite interactions of adherent versus nonadherent T. vaginalis isolates to hVECs. The binding of the TH17 adherent isolate to hVECs exhibited an initial discrete phase followed by an aggregation phase inhibited by lactose. T. vaginalis infection immediately induced surface expression of galectin-1 and -3, with extracellular amounts in the spent medium initially decreasing and then increasing thereafter over the next 60 min. Extracellular galectin-1 and -3 were detected on the parasite surface but only the TH17 adherent isolate could uptake galectin-3 via the lysosomes. Only the adherent isolate could morphologically transform from the round-up flagellate with numerous transient protrusions into a flat amoeboid form on contact with the solid surface. Cytochalasin D challenge revealed that actin organization was essential to parasite morphogenesis and cytoadherence. Real-time microscopy showed that parasite exploring and anchoring on hVECs via the axostyle may be required for initial cytoadherence. Together, the parasite cytoskeleton behaviors may collaborate with cell surface adhesion molecules for cytoadherence. The nonadherent isolate migrated faster than the adherent isolate, with motility transiently increasing in the presence of hVECs. Meanwhile, differential histone acetylation was detected between the two isolates. Also, TH17 without Mycoplasma symbiosis suggests that symbiont might not determine TH17 innate cytoadherence. Our findings regarding distinctive host-parasite interactions of the isolates may provide novel insights into T. vaginalis infection.

PIP2 regulating calcium signal modulates actin cytoskeleton-dependent cytoadherence and cytolytic capacity in the protozoan parasite Trichomonas vaginalis

“…Recently, we found that actin cytoskeleton activity is involved in the morphogenesis and cytoadherence of T . vaginalis [ 27 , 28 ], prompting us to investigate the upstream signaling. T1 is a less adherent isolate with only the flagellate form freely swimming by flagellar motoring in suspension.…”

“…Flagellate-amoeboid transition is critical for T . vaginalis cytoadherence [ 27 , 28 ]. TH17 flagellate trophozoites were cultured on a glass slide to trigger contact-dependent amoeboid morphogenesis ( Fig 3A , S1 Movie ) and after 30 minutes, ~80% of the TH17 non-transfectant or HA- Tv PI4P5K transfectant trophozoites transformed into the amoeboid form but only ~40% of the K136A mutant transformed ( Fig 3B ).…”

“…Previously, we demonstrated that actin polymerization is crucial in T . vaginalis flagellate-amoeboid transition [ 27 , 28 ], so we further examined whether PIP 2 signaling regulates amoeboid morphogenesis through actin cytoskeleton organization. The transfectants equally overexpressing HA- Tv PI4P5K Wt and K136A ( Fig 5A ) were fractionated into the supernatant (G-actin) and pellet (F-actin) to evaluate actin polymerization.…”

“…All isolates were deposited in the biosafety chamber of our institute for research only (National Taiwan University, College of Medicine). In contrast to the T1, G3, and TH17 experimental isolates [ 27 , 28 ], the fresh clinical isolates cultured short-term for weeks rather than years may preserve more intrinsic virulence. Human vagina epithelium cell ( h VECs) was cultured in keratinocyte serum-free medium (Gibco) at 37°C with 5% CO 2 .…”

“…Recent studies have demonstrated that the actin-cytoskeleton-mediated amoeboid morphogenesis capacity biologically correlates with cytoadherence and migration crucial for T . vaginalis colonizing host [ 27 , 28 ].…”